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Scaly skin in EFAD blamed on deficiency in cancer promoting Omega-6 metabolite
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Taka
Jul 6, 2012, 9:52:48 AM7/6/12
to
"Linoleic acid is the precursor 13-hydroxyoctadecadienoic acid (13-
HODE), an anti-hyperproliferative compound in epidermis. In EFA
deficiency, the level of 13-HODE in epidermis is decreased, resulting
in scaly skin."
"Linoleic acid is an essential component of ceramides, a key group of
compounds in the lipid barrier structure of skin. Replacing linoleic
acid with other fatty acids (e.g. oleic acid) in ceramides leads to an
increased permeability, sensitivity, and trans-epidermal water loss
(dryness) of skin"
SOURCE: http://www.nyscc.org/cosmetiscope/archive/tech1005.html
"13-HODE is the principle hydroxylated fatty acid in human psoriatic
skin scales, with a mean concentration of 17 ng/mg"
SOURCE: http://www.caymanchem.com/app/template/Product.vm/catalog/38600
------------------------------
http://www.caymanchem.com/app/template/Article.vm/article/2137
HODE), an anti-hyperproliferative compound in epidermis. In EFA
deficiency, the level of 13-HODE in epidermis is decreased, resulting
in scaly skin."
"Linoleic acid is an essential component of ceramides, a key group of
compounds in the lipid barrier structure of skin. Replacing linoleic
acid with other fatty acids (e.g. oleic acid) in ceramides leads to an
increased permeability, sensitivity, and trans-epidermal water loss
(dryness) of skin"
SOURCE: http://www.nyscc.org/cosmetiscope/archive/tech1005.html
"13-HODE is the principle hydroxylated fatty acid in human psoriatic
skin scales, with a mean concentration of 17 ng/mg"
SOURCE: http://www.caymanchem.com/app/template/Product.vm/catalog/38600
------------------------------
http://www.caymanchem.com/app/template/Article.vm/article/2137
Taka
Jul 6, 2012, 9:59:42 AM7/6/12
to
Circadian Stage-Dependent Metabolic and Anticancer Effects of
Melatonin in Rats and Women and Their Disruption by Light at Night
David E. Blask, Ph.D.,M.D1., Robert T. Dauchy, B.A.1, George C.
Brainard, Ph.D2., and John Hanifin, B.S.2, 1Tulane University School
of Medicine, New Orleans, LA and 2Thomas Jefferson University,
Philadelphia, PA
The circadian production of melatonin by the pineal gland during the
night provides an inhibitory signal to tissue-isolated steroid
receptor negative (SR-) MCF-7 human breast cancer xenografts in female
nude rats. A central mechanism for melatonin’s anticancer effects in
vivo involves a melatonin receptor-mediated inhibition of linoleic
acid (LA) uptake and its metabolism to mitogenically active 13-
hydroxyoctadecadienoic acid (13-HODE). These human breast cancer
xenografts exhibit robust circadian rhythms of glucose uptake and
metabolism to lactic acid, LA uptake and metabolism to 13-HODE, cAMP
formation, and proliferative activity. Exposure of xenograft-bearing
rats to 0.08 uW/cm2 (0.2 lux) of dim, polychromatic light at night
suppresses melatonin while the nocturnal circadian rhythm of feeding
and drinking behavior is preserved under these conditions. Dim light
at night results in the elimination or modification of these circadian
rhythms culminating in unfettered tumor glucose, and LA uptake and
metabolism, cAMP formation, [3H]thymidine incorporation into DNA and
tumor growth. Similar effects occur in xenografts perfused with blood
from healthy female subjects during the dark and after exposure to
bright (2800 lux) polychromatic light at night.
MORE AT: http://www.nyas.org/Events/Detail.aspx?cid=4d8d0e99-947b-47ff-86db-610dc127cabf
Cancer Res. 1999 Sep 15;59(18):4693-701.
Melatonin inhibition of cancer growth in vivo involves suppression of
tumor fatty acid metabolism via melatonin receptor-mediated signal
transduction events.
Blask DE, Sauer LA, Dauchy RT, Holowachuk EW, Ruhoff MS, Kopff HS.
SourceLaboratory of Experimental Neuroendocrinology/Oncology, Bassett
Research Institute, Cooperstown, New York 13326-1394, USA.
The growth of rat hepatoma 7288CTC in vivo is stimulated by the uptake
of linoleic acid (LA) and its metabolism to 13-hydroxyoctadecadienoic
acid (13-HODE), an important mitogenic signaling molecule within this
tumor. Conversely, the growth of a variety of experimental cancers in
vivo is inhibited by either physiological or pharmacological levels of
the pineal gland hormone melatonin, although the mechanism(s) are
unknown. We tested the hypothesis that the mechanism of melatonin's
anticancer action in vivo involves the inhibition of tumor LA uptake
and metabolism to 13-HODE in hepatoma 7288CTC. Tumor uptake of LA and
release of 13-HODE, measured in tissue-isolated rat hepatoma 7288CTC
at 4-h intervals over a 24-h period, were highest during the light
phase and lowest during the mid-dark phase, when plasma melatonin
levels were lowest and highest, respectively. Pinealectomy eliminated
this rhythm of tumor LA uptake and 13-HODE production, indicating that
it was driven by the circadian melatonin rhythm. Perfusion of tissue-
isolated tumors in situ with melatonin (1 nM) rapidly and reversibly
inhibited the uptake of plasma fatty acids (FAs), including LA, and
its metabolism to 13-HODE. These inhibitory effects of melatonin on
tumor FA uptake and 13-HODE release were completely reversed by
perfusion of tumors in situ with melatonin receptor antagonist
S-20928, pertussis toxin, forskolin, or 8-bromo-cAMP. Perfusion of
tumors in situ with melatonin also decreased tumor [3H]thymidine
incorporation and DNA content; these effects on DNA synthesis were
also prevented by the coperfusion of tumors with melatonin and
S-20928, pertussis toxin, forskolin, 8-Br-cAMP, or 13-HODE.
Pinealectomy stimulated tumor growth, LA uptake and metabolism to 13-
HODE, and FA storage in hepatoma 7288CTC, whereas melatonin
administration (200 microg/day) was inhibitory in vivo. Northern blot
analysis revealed that, compared with normal liver tissue, hepatoma
7288CTC overexpressed mRNA transcripts for a plasma membrane-
associated FA transport protein (FATP). FATP mRNA expression was
unaffected by the treatment of tumor-bearing rats with daily afternoon
melatonin injections or exposure to constant light. These results
support a novel mechanism of tumor growth inhibition by melatonin
involving a melatonin receptor-mediated suppression of cAMP levels,
resulting in diminished tumor FA transport, possibly via decreased
FATP function. The inhibition of these signal transduction events by
melatonin culminates in the suppression of LA uptake, LA metabolism to
the mitogenic signaling molecule 13-HODE, and cancer growth.
PMID:10493527
Integr Cancer Ther. 2009 Dec;8(4):347-53.
Circadian stage-dependent inhibition of human breast cancer metabolism
and growth by the nocturnal melatonin signal: consequences of its
disruption by light at night in rats and women.
Blask DE, Dauchy RT, Brainard GC, Hanifin JP.
SourceTulane Cancer Center and Louisiana Cancer Research Consortium,
Tulane University School of Medicine, New Orleans, LA 70112, USA.
The circadian production of melatonin by the pineal gland during the
night provides an inhibitory signal to tissue-isolated steroid
receptor SR+ and - MCF-7 human breast cancer xenografts in female nude
rats. A pivotal mechanism for melatonin's anticancer effects in vivo
involves a melatonin receptor-mediated inhibition of linoleic acid
(LA) uptake and its metabolism to mitogenically active 13-
hydroxyoctadecadienoic acid (13-HODE). Exposure of (SR-) xenograft-
bearing rats to increasing intensities of polychromatic white light at
night suppresses melatonin while increasing tumor growth rates, DNA
content, [3H]thymidine incorporation into DNA, LA uptake, 13-HODE
formation, cAMP levels and ERK1/2 activation a dose-dependent manner.
Similar effects occur in SR- human breast cancer xenografts perfused
in situ with melatonin-depleted blood from healthy female subjects
after their exposure to a single bright intensity (2800 lux) of
polychromatic light at night. Additionally, SR- human breast cancer
xenografts exhibit robust circadian rhythms of LA uptake, 13-HODE
formation and proliferative activity. Exposure of xenograft-bearing
rats to dim light at night results in the complete elimination of
these rhythms which culminates in unfettered, high rates of tumor
metabolism and growth. The organization of tumor metabolism and growth
within circadian time structure by the oncostatic melatonin signal
helps create a balance between the cancer and its host that is
disrupted by host exposure to light at night. This biological
mechanism may partially explain the higher risk of breast and other
cancers in women working rotating night shifts and possibly others who
also experience prolonged exposure to light at night.
PMID:20042410
Melatonin in Rats and Women and Their Disruption by Light at Night
David E. Blask, Ph.D.,M.D1., Robert T. Dauchy, B.A.1, George C.
Brainard, Ph.D2., and John Hanifin, B.S.2, 1Tulane University School
of Medicine, New Orleans, LA and 2Thomas Jefferson University,
Philadelphia, PA
The circadian production of melatonin by the pineal gland during the
night provides an inhibitory signal to tissue-isolated steroid
receptor negative (SR-) MCF-7 human breast cancer xenografts in female
nude rats. A central mechanism for melatonin’s anticancer effects in
vivo involves a melatonin receptor-mediated inhibition of linoleic
acid (LA) uptake and its metabolism to mitogenically active 13-
hydroxyoctadecadienoic acid (13-HODE). These human breast cancer
xenografts exhibit robust circadian rhythms of glucose uptake and
metabolism to lactic acid, LA uptake and metabolism to 13-HODE, cAMP
formation, and proliferative activity. Exposure of xenograft-bearing
rats to 0.08 uW/cm2 (0.2 lux) of dim, polychromatic light at night
suppresses melatonin while the nocturnal circadian rhythm of feeding
and drinking behavior is preserved under these conditions. Dim light
at night results in the elimination or modification of these circadian
rhythms culminating in unfettered tumor glucose, and LA uptake and
metabolism, cAMP formation, [3H]thymidine incorporation into DNA and
tumor growth. Similar effects occur in xenografts perfused with blood
from healthy female subjects during the dark and after exposure to
bright (2800 lux) polychromatic light at night.
MORE AT: http://www.nyas.org/Events/Detail.aspx?cid=4d8d0e99-947b-47ff-86db-610dc127cabf
Cancer Res. 1999 Sep 15;59(18):4693-701.
Melatonin inhibition of cancer growth in vivo involves suppression of
tumor fatty acid metabolism via melatonin receptor-mediated signal
transduction events.
Blask DE, Sauer LA, Dauchy RT, Holowachuk EW, Ruhoff MS, Kopff HS.
SourceLaboratory of Experimental Neuroendocrinology/Oncology, Bassett
Research Institute, Cooperstown, New York 13326-1394, USA.
The growth of rat hepatoma 7288CTC in vivo is stimulated by the uptake
of linoleic acid (LA) and its metabolism to 13-hydroxyoctadecadienoic
acid (13-HODE), an important mitogenic signaling molecule within this
tumor. Conversely, the growth of a variety of experimental cancers in
vivo is inhibited by either physiological or pharmacological levels of
the pineal gland hormone melatonin, although the mechanism(s) are
unknown. We tested the hypothesis that the mechanism of melatonin's
anticancer action in vivo involves the inhibition of tumor LA uptake
and metabolism to 13-HODE in hepatoma 7288CTC. Tumor uptake of LA and
release of 13-HODE, measured in tissue-isolated rat hepatoma 7288CTC
at 4-h intervals over a 24-h period, were highest during the light
phase and lowest during the mid-dark phase, when plasma melatonin
levels were lowest and highest, respectively. Pinealectomy eliminated
this rhythm of tumor LA uptake and 13-HODE production, indicating that
it was driven by the circadian melatonin rhythm. Perfusion of tissue-
isolated tumors in situ with melatonin (1 nM) rapidly and reversibly
inhibited the uptake of plasma fatty acids (FAs), including LA, and
its metabolism to 13-HODE. These inhibitory effects of melatonin on
tumor FA uptake and 13-HODE release were completely reversed by
perfusion of tumors in situ with melatonin receptor antagonist
S-20928, pertussis toxin, forskolin, or 8-bromo-cAMP. Perfusion of
tumors in situ with melatonin also decreased tumor [3H]thymidine
incorporation and DNA content; these effects on DNA synthesis were
also prevented by the coperfusion of tumors with melatonin and
S-20928, pertussis toxin, forskolin, 8-Br-cAMP, or 13-HODE.
Pinealectomy stimulated tumor growth, LA uptake and metabolism to 13-
HODE, and FA storage in hepatoma 7288CTC, whereas melatonin
administration (200 microg/day) was inhibitory in vivo. Northern blot
analysis revealed that, compared with normal liver tissue, hepatoma
7288CTC overexpressed mRNA transcripts for a plasma membrane-
associated FA transport protein (FATP). FATP mRNA expression was
unaffected by the treatment of tumor-bearing rats with daily afternoon
melatonin injections or exposure to constant light. These results
support a novel mechanism of tumor growth inhibition by melatonin
involving a melatonin receptor-mediated suppression of cAMP levels,
resulting in diminished tumor FA transport, possibly via decreased
FATP function. The inhibition of these signal transduction events by
melatonin culminates in the suppression of LA uptake, LA metabolism to
the mitogenic signaling molecule 13-HODE, and cancer growth.
PMID:10493527
Integr Cancer Ther. 2009 Dec;8(4):347-53.
Circadian stage-dependent inhibition of human breast cancer metabolism
and growth by the nocturnal melatonin signal: consequences of its
disruption by light at night in rats and women.
Blask DE, Dauchy RT, Brainard GC, Hanifin JP.
SourceTulane Cancer Center and Louisiana Cancer Research Consortium,
Tulane University School of Medicine, New Orleans, LA 70112, USA.
The circadian production of melatonin by the pineal gland during the
night provides an inhibitory signal to tissue-isolated steroid
receptor SR+ and - MCF-7 human breast cancer xenografts in female nude
rats. A pivotal mechanism for melatonin's anticancer effects in vivo
involves a melatonin receptor-mediated inhibition of linoleic acid
(LA) uptake and its metabolism to mitogenically active 13-
hydroxyoctadecadienoic acid (13-HODE). Exposure of (SR-) xenograft-
bearing rats to increasing intensities of polychromatic white light at
night suppresses melatonin while increasing tumor growth rates, DNA
content, [3H]thymidine incorporation into DNA, LA uptake, 13-HODE
formation, cAMP levels and ERK1/2 activation a dose-dependent manner.
Similar effects occur in SR- human breast cancer xenografts perfused
in situ with melatonin-depleted blood from healthy female subjects
after their exposure to a single bright intensity (2800 lux) of
polychromatic light at night. Additionally, SR- human breast cancer
xenografts exhibit robust circadian rhythms of LA uptake, 13-HODE
formation and proliferative activity. Exposure of xenograft-bearing
rats to dim light at night results in the complete elimination of
these rhythms which culminates in unfettered, high rates of tumor
metabolism and growth. The organization of tumor metabolism and growth
within circadian time structure by the oncostatic melatonin signal
helps create a balance between the cancer and its host that is
disrupted by host exposure to light at night. This biological
mechanism may partially explain the higher risk of breast and other
cancers in women working rotating night shifts and possibly others who
also experience prolonged exposure to light at night.
PMID:20042410
John H. Gohde
Jul 6, 2012, 10:36:58 AM7/6/12
to
I love light. :)
montygraham
Jul 7, 2012, 12:22:51 AM7/7/12
to
Let's be scientific here: the same fatty acid that can be used to
promote inflammation/cancer can be used to create an oil painting.
When it's used for an oil painting, it becomes chemically stable
(though free radicals were involved in part of the process). When I
decided to have AA replaced by Mead acid, I noticed dryness and when I
drank more water than usual the "problem" quickly resolved. By
contrast, with AA in my cells, I had problems with dandruff,
Chalazions, and a keloid, as well as frequent minor rashes (along with
other problems not related to the skin). If one looks for "symptoms"
one can usually find some, because few if any humans are physically
perfect. Science demands properly controlled studies. Anecdotal
evidence is fine if you are using it to formulate a hypothesis, but
then the hypothesis has to be tested appropriately. This has never
been done, IMO, withe these kinds of "EFA" claims.
promote inflammation/cancer can be used to create an oil painting.
When it's used for an oil painting, it becomes chemically stable
(though free radicals were involved in part of the process). When I
decided to have AA replaced by Mead acid, I noticed dryness and when I
drank more water than usual the "problem" quickly resolved. By
contrast, with AA in my cells, I had problems with dandruff,
Chalazions, and a keloid, as well as frequent minor rashes (along with
other problems not related to the skin). If one looks for "symptoms"
one can usually find some, because few if any humans are physically
perfect. Science demands properly controlled studies. Anecdotal
evidence is fine if you are using it to formulate a hypothesis, but
then the hypothesis has to be tested appropriately. This has never
been done, IMO, withe these kinds of "EFA" claims.
John H. Gohde
Jul 7, 2012, 6:28:59 AM7/7/12
to
Mead acid?
Loony
Jul 7, 2012, 6:35:58 AM7/7/12
to
Hello Taka,
Thank you for your good work in these Newsgroups.
I have been a vegetarian for many decades and I now am getting a sense
that I need vegetarian omegas. My skin, nails, etc. are suffering.
Please advise of reasonably priced supplements.
Thx.
Thank you for your good work in these Newsgroups.
I have been a vegetarian for many decades and I now am getting a sense
that I need vegetarian omegas. My skin, nails, etc. are suffering.
Please advise of reasonably priced supplements.
Thx.
Taka
Jul 7, 2012, 8:52:27 AM7/7/12
to
On Jul 7, 7:35 pm, Loony <Lo...@nowhere.con> wrote:
> Hello Taka,
>
> Thank you for your good work in these Newsgroups.
>
> I have been a vegetarian for many decades and I now am getting a sense
> that I need vegetarian omegas. My skin, nails, etc. are suffering.
>
> Please advise of reasonably priced supplements.
>
> Thx.
Gelatin
> Hello Taka,
>
> Thank you for your good work in these Newsgroups.
>
> I have been a vegetarian for many decades and I now am getting a sense
> that I need vegetarian omegas. My skin, nails, etc. are suffering.
>
> Please advise of reasonably priced supplements.
>
> Thx.
Taka
Jul 7, 2012, 8:54:22 AM7/7/12
to
On Jul 7, 7:28 pm, "John H. Gohde" <john.h.go...@gmail.com> wrote:
> What is Hell, if it wouldNOT be eating a montygraham diet full of
> Mead acid?
You don't understand a thing here ...
> What is Hell, if it wouldNOT be eating a montygraham diet full of
> Mead acid?
John H. Gohde
Jul 7, 2012, 10:15:54 AM7/7/12
to
will fade away quite fast as immortal science lives on forever off of
the blood of its victims. That sentiment is fine with me, just as
long as it is NOT my blood. :)
Loony
Jul 7, 2012, 10:48:26 AM7/7/12
to
Loony
Jul 7, 2012, 10:50:37 AM7/7/12
to
flavorless solid substance, derived from the collagen mainly inside pig
skin (hide) and cattle bones.
Taka
Jul 7, 2012, 11:32:14 AM7/7/12
to
On Jul 7, 11:50 pm, Loony <Lo...@nowhere.con> wrote:
> >>> I have been a vegetarian for many decades and I now am getting a sense
> >>> that I need vegetarian omegas. My skin, nails, etc. are suffering.
This is not from "essential fatty" acid deficiency. IMO as a
> >>> I have been a vegetarian for many decades and I now am getting a sense
> >>> that I need vegetarian omegas. My skin, nails, etc. are suffering.
vegetarian, you are not getting enough other macro (and perhaps micro)
nutrients such as high quality protein. You may add some eggs or
dairy but the best protein for your nails etc. is gelatin. Eating
some nuts or avogados provides plenty of EFAs.
http://raypeat.com/articles/articles/gelatin.shtml
> >>> Please advise of reasonably priced supplements.
>
> >>> Thx.
>
> >> Gelatin
>
> > Is this vegetarian?
caucasians) adapted later to consuming meat especially bones and
connective tissue (collagen). Read RayPeat above, he is one of the
most intelligent scientists I have ever seen. You may base your diet
on tropical fruits but I would stay away from grains which are primary
food for birds (and you could be celiac) and beans which contain
antinutrients such as goitrogens. Potato and root vegetable is OK.
If you want to supplement something, try B vitamins e.g. in the form
of brewery yeast. You may be deficient in some of them such as B12.
Taka
Taka
Jul 7, 2012, 11:39:59 AM7/7/12
to
On Jul 8, 12:32 am, Taka <taka0...@gmail.com> wrote:
> If you want to supplement something, try B vitamins e.g. in the form
> of brewery yeast. You may be deficient in some of them such as B12.
And speaking of EFAs, VitB6 is important cofactor of the enzyme
> If you want to supplement something, try B vitamins e.g. in the form
> of brewery yeast. You may be deficient in some of them such as B12.
desaturase which makes the essential long chain PUFAs from their plant
precursors or oleic acid (in the case of Mead acid). Rather than
swallowing fish oil pills try taking Vitamin B6.
Taka
montygraham
Jul 8, 2012, 9:33:24 PM7/8/12
to
My fingernails got soft after years on a vegan diet and a few years
taking omega 3 supplements. The only thing that worked was to take
tiny amounts of gelatin each day. It took a few months but since then
(about 7 years ago) my nails have been so hard and sharp that I have
to be careful when I scratch myself. You nails are not made out of
fatty acids; they are made out of certain kinds of amino acids
(organized in a specific way).
taking omega 3 supplements. The only thing that worked was to take
tiny amounts of gelatin each day. It took a few months but since then
(about 7 years ago) my nails have been so hard and sharp that I have
to be careful when I scratch myself. You nails are not made out of
fatty acids; they are made out of certain kinds of amino acids
(organized in a specific way).
Doug Freyburger
Jul 9, 2012, 3:10:06 PM7/9/12
to
product) for this purpose? For a lot of uses agar agar works as a
substitute for gelatin and I wondered about this use.
Taka
Jul 9, 2012, 9:21:01 PM7/9/12
to
get you poop.
Taka
Robert Miles
Jul 30, 2012, 12:20:28 PM7/30/12
to
You might consider growing a vegetable called purslane - it produces
all the major types of omega-3. It is often used as a wild food
in Europe, but is generally considered a weed in the US. Supermarkets
usually sell it only in a mixture called mesclun salad. Farmers'
markets are more likely to have some available.
Omega-6 is easier to find - most of the vegetable oils available
contain some.
all the major types of omega-3. It is often used as a wild food
in Europe, but is generally considered a weed in the US. Supermarkets
usually sell it only in a mixture called mesclun salad. Farmers'
markets are more likely to have some available.
Omega-6 is easier to find - most of the vegetable oils available
contain some.
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